The cardiac parasympathetic fibers originate in the medulla oblongata, in cells that lie in the dorsal motor nucleus of the vagus nerve or in the nucleus ambiguus (see ). In humans, centrifugal vagal fibers pass inferiorly through the neck near the common carotid arteries and then through the mediastinum to synapse with postganglionic vagal cells. These cells are located either on the epicardial surface or within the walls of the heart. Most of the vagal ganglion cells are located in epicardial fat pads near the SA and atrioventricular (AV) nodes.
The right and left vagus nerves are distributed to different cardiac structures. The right vagus nerve affects the SA node predominantly; stimulation of this nerve slows SA nodal firing and can even stop the firing for several seconds. The left vagus nerve mainly inhibits AV conduction tissue to produce various degrees of AV block (see ). However, the distribution of the efferent vagal fibers is overlapping in such a way that left vagal stimulation also •Fig. 18.3 Changes in Heart Rate When the Vagus and Cardiac
Sympathetic Nerves Are Stimulated Simultaneously. Thesympa depresses the SA node and right vagal stimulation impedes AV conduction.
The SA and AV nodes are rich in acetylcholinesterase, an enzyme that rapidly hydrolyzes the neurotransmitter acetylcholine (ACh). The effects of a given vagal stimulus decay very quickly (
Fig. 18.2A ) when vagal stimulation is discontinued because ACh is rapidly destroyed. In addition, vagal effects on SA and AV nodal function have a very short latency (≈50 to 100 msec) because the ACh released quickly activates special ACh-regulated potassium (KACh) channels in the cardiac cells. These channels open quickly because the muscarinic receptor is coupled directly to the KACh channel by a guanine nucleotide–binding protein. These two features of the vagus nerves—brief latency and rapid theticnerveswerestimulatedat0,2,and4Hzinthepresenceofvagalnervestimulation(Vag)at0,4,and8Hz.(ModifiedfromLevyMN,ZieskeH.J Appl Physiol. 1969;27:465.) decay of the response—enable them to exert beat-by-beat control of SA and AV nodal function.
Parasympathetic influences usually predominate over sympathetic effects at the SA node, as shown in
Fig. 18.3 . When the frequency of sympathetic stimulation increases from 0 to 4 Hz, the heart rate increases by approximately 80 beats per minute in the absence of vagal nerve stimulation (0 Hz). However, when the vagus nerves are stimulated at 8 Hz, increasing the sympathetic stimulation frequency from 0 to 4 Hz has only a negligible influence on heart rate.
The cardiac sympathetic fibers originate in the intermediolateral columns of the upper five or six thoracic segments and the lower one or two cervical segments of the spinal cord (see ). These fibers emerge from the spinal column through the white communicating branches and enter the paravertebral chains of ganglia. The preganglionic and postganglionic neurons synapse mainly in the stellate or middle cervical ganglia, depending on the species. In the mediastinum, postganglionic sympathetic and preganglionic parasympathetic fibers join to form a complicated plexus of mixed efferent nerves to the heart.
The postganglionic cardiac sympathetic fibers in this plexus approach the base of the heart along the adventitial surface of the great vessels. From the base of the heart, these fibers are distributed to the various chambers as an extensive epicardial plexus. They then penetrate the myocardium, usually accompanying the coronary vessels.
In contrast to abrupt termination of the response after vagal activity, the effects of sympathetic stimulation decay gradually after stimulation is stopped (see